Seth Lipka1, Ambuj Kumar, Joel E Richter. 1. *Division of Digestive Diseases and Nutrition †Department of Medicine, Division of Evidence-based Medicine and Outcomes Research ‡Division of Digestive Diseases and Nutrition, Joy McCann Culverhouse Center for Swallowing Disorders, University of South Florida Morsani College of Medicine, Tampa, FL.
Abstract
GOALS: Endoscopic features of eosinophilic esophagitis (EoE) are variable with at least 2 phenotypes. The goal of this study was to classify adult EoE patients based on esophageal phenotype and diameter, and assess an association between demographical and clinical histories to define EoE phenotypes and overall disease progression. METHODS: All consecutive patients with a confirmed diagnosis of EoE from 1988 to 2013 treated at University of South Florida were included. Patients were grouped into inflammatory or fibrostenotic phenotype, and further characterized by esophageal diameter: group 1 (6 to 9.9 mm), group 2 (10 to 16.9 mm), and group 3 (>17 mm-control). Significance level was set at 5%. RESULTS: Sixty-four adult patients met inclusion criteria. Sixty-one percent of patients (39/64) were defined as fibrostenotic and 39% (25/64) as inflammatory phenotype. There was a significant difference in mean time of delayed diagnosis in patients with <10 mm esophageal diameter (14.8 y) and patients with a diameter of 10 to 16.9 mm (11.1 y) compared with patients with an esophageal diameter of ≥17 mm (5 y); P=0.002 and 0.006, respectively. Patients on aspirin with delayed diagnosis (>7 y) were significantly more likely to present with strictures (<10 mm) compared with nonaspirin users [odds ratio (OR=7.0; 95% confidence interval (CI), 7.2-31.3; P=0.008]. Similar results were found with non-steroid anti-inflammatory drugs, smoking, and alcohol (OR=6.4; 95% CI, 1.6-26.4; P=0.01, OR=5.2; 95% CI, 1.4-20.1; P=0.02, and OR=6.4; 95% CI, 1.6-26.0; P=0.009), respectively. CONCLUSIONS: In our US population, a delay in diagnosis was shown to be associated with stricture formation in EoE confirming the Swiss experience. The results show the importance of reducing the diagnostic delay in EoE as there appears to be progression to fibrosis over time, aggravated by common medications and social habits.
GOALS: Endoscopic features of eosinophilic esophagitis (EoE) are variable with at least 2 phenotypes. The goal of this study was to classify adult EoE patients based on esophageal phenotype and diameter, and assess an association between demographical and clinical histories to define EoE phenotypes and overall disease progression. METHODS: All consecutive patients with a confirmed diagnosis of EoE from 1988 to 2013 treated at University of South Florida were included. Patients were grouped into inflammatory or fibrostenotic phenotype, and further characterized by esophageal diameter: group 1 (6 to 9.9 mm), group 2 (10 to 16.9 mm), and group 3 (>17 mm-control). Significance level was set at 5%. RESULTS: Sixty-four adult patients met inclusion criteria. Sixty-one percent of patients (39/64) were defined as fibrostenotic and 39% (25/64) as inflammatory phenotype. There was a significant difference in mean time of delayed diagnosis in patients with <10 mm esophageal diameter (14.8 y) and patients with a diameter of 10 to 16.9 mm (11.1 y) compared with patients with an esophageal diameter of ≥17 mm (5 y); P=0.002 and 0.006, respectively. Patients on aspirin with delayed diagnosis (>7 y) were significantly more likely to present with strictures (<10 mm) compared with nonaspirin users [odds ratio (OR=7.0; 95% confidence interval (CI), 7.2-31.3; P=0.008]. Similar results were found with non-steroid anti-inflammatory drugs, smoking, and alcohol (OR=6.4; 95% CI, 1.6-26.4; P=0.01, OR=5.2; 95% CI, 1.4-20.1; P=0.02, and OR=6.4; 95% CI, 1.6-26.0; P=0.009), respectively. CONCLUSIONS: In our US population, a delay in diagnosis was shown to be associated with stricture formation in EoE confirming the Swiss experience. The results show the importance of reducing the diagnostic delay in EoE as there appears to be progression to fibrosis over time, aggravated by common medications and social habits.
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